4.2 Article

Scriptaid inhibits cell survival, cell cycle, and promotes apoptosis in multiple myeloma via epigenetic regulation of p21

Journal

EXPERIMENTAL HEMATOLOGY
Volume 60, Issue -, Pages 63-72

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.exphem.2017.12.012

Keywords

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Funding

  1. National Natural Science Foundation of China [81600173, 81400127]
  2. Natural Science Foundation of Jiangsu Province [BK20160230]
  3. Postdoctoral Science Foundation of China [2016M601895]
  4. Postdoctoral Science Foundation of Jiangsu Province [1601092B]
  5. Science and Technology Special Project in Clinical Medicine of Jiangsu Province [BL2013010]
  6. Jiangsu Provincial Key Research and Development Program [BE2017638]

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Multiple myeloma (MM) is an extremely serious plasma cell malignancy. Despite the recent introduction of chemotherapies such as bortezomib and lenalidomide, it remains an incurable disease due to the high rate of relapse and the development of drug resistance. Epigenetic regulation is closely related to MM progression, but the epigenetic modification mechanism of MM cell apoptosis has remained unclear. As a novel histone deacetylase inhibitor (HDACi), Scriptaid's possible roles in MM progression have not been explored. Herein, we found that Scriptaid decreased several human MM cell viabilities in a dose-dependent manner. Scriptaid was also able to dose dependently and significantly induce MM cell cycle arrest at the G(2)/M phase. Moreover, Scriptaid facilitates p21 transcriptional activities by mediating H3Ac gene-activated modification, eventually leading to MM cell apoptosis. Overall, our results show that Scriptaid is an inducer of MM cell death, suggesting the possibility for Scriptaid-mediated therapeutics to cure refractory/relapsed MM. (C) 2018 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.

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